Clinical Review Article

Shock with Jugular Venous Distention

Ketul Chauhan, MD
Douglas D. Schocken, MD

hock is a frequently encountered, life-threatening

S clinical syndrome that can be readily diagnosed at

the bedside by observing hypotension and signs
and symptoms of hypoperfusion (eg, mental sta-
tus changes, weakness, cyanosis, dyspnea, and oliguria).
There is a wide range of causes of shock, but few presen-
TAKE HOME POINTS

Examining the neck for jugular venous distention

(JVD) is critical for the evaluation of all patients
who present with shock because, while shock has a
tations include jugular venous distention (JVD). The broad differential diagnosis, there are relatively few
common pathophysiology in the differential diagnosis of presentations that include JVD.
shock with JVD (Table) is inhibition of right ventricular Echocardiography can be helpful in differentiating
outflow and/or right ventricular filling. This process among specific etiologies for shock with JVD.
translates into decreased right atrial emptying, as mani- In postoperative cardiothoracic surgery patients,
fested by JVD. A systematic approach to the presentation shock with JVD should trigger a differential diag-
of shock with JVD can prevent unhelpful diagnostic test- nosis that includes pericardial tamponade, pericar-
ing and loss of valuable time (Figure 1). An approach dial clot, tension pneumothorax, and cardiac her-
that includes a thorough history and physical examina- niation.
tion, with echocardiography as an essential diagnostic All acute inferior wall myocardial infarctions
modality, can differentiate among most underlying especially those with hypotension and JVD
problems and help direct an appropriate management should be considered as involving the right
plan (Figure 2). This article provides an overview of con- ventricle and should prompt additional electro-
ditions associated with the presentation of shock and cardiograms with right-sided precordial leads
JVD, with a focus on important features of the diagnosis (looking for ST elevation in leads V3r and V4r).
and management of these conditions.

END-STAGE CONGESTIVE HEART FAILURE

The most common etiologies of heart failure include
coronary artery disease, hypertension, valvular heart dis- tion, ventricular gallop, Cheyne-Stokes breathing, ele-
ease, cardiomyopathy, myocarditis, and congenital heart vated jugular venous pressure, and peripheral vascular
disease. Heart failure begins with impaired ventricular congestion. Chest radiography may confirm pulmo-
function that results in decreased cardiac output. Re- nary vascular and alveolar congestion with findings of
duced output, in turn, activates neuroendocrine systems Kerleys B lines and prominence of pulmonary vessels,
(renin-angiotensin system, arginine-vasopressin system, along with evidence of cardiomegaly with or without
sympathetic nervous system) that produce systemic vaso- pleural effusion. Echocardiography is an excellent ini-
constriction, which results in increased afterload and tial tool for evaluating these patients for structural and
further decreases cardiac performance. Decreasing car- functional abnormalities. Measurement of brain natri-
diac output presents as shock, and progressive fluid uretic peptide levels has become an established diag-
retention due to neurohormonal activation causes an nostic test for evaluating patients with suspected heart
increase in right-sided pressure and JVD.1 failure.2

Diagnosis
The presentation and hemodynamics of end-stage
Dr. Chauhan is a fellow in cardiovascular disease, and Dr. Schocken is
heart failure with systolic dysfunction are generally uni- a professor of medicine; both are at the Division of Cardiovascular
form, regardless of the initial pathology. Patients pre- Disease, Department of Internal Medicine, University of South Florida,
sent with dyspnea, hypotension, pulmonary conges- College of Medicine, Tampa, FL.

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 Chauhan & Schocken : Shock with JVD : pp. 17 24, 29

Table. Differential Diagnosis of Shock with Jugular Venous of right ventricular MI is proximal occlusion of a domi-
Distension nant right coronary artery.4
End-stage heart failure Massive pulmonary embolism Patients with right ventricular MI usually present
Acute myocardial infarction Right atrial or ventricular
with a triad of hypotension, elevated jugular venous
thrombus pressure, and clear lung sounds. These patients may
Cardiac tamponade
Cardiac tumors also complain of chest pain, nausea, dizziness, tachyp-
Pericardial thrombus
Cardiac herniation
nea, and tachycardia. Acute right-sided MI leads to de-
Constrictive pericarditis
creased right ventricular compliance, reduced stroke
Tension pneumothorax volume, reduced preload for the left ventricle, and, as a
result, reduced cardiac output. At the same time, acute
right ventricular dilation may occur along with segmen-
Treatment tal wall motion abnormalities.5
Patients in advanced heart failure with New York
Heart Association class III and IV symptoms should be Diagnostic Modalities
treated with angiotensin-converting enzyme inhibitors, Clinical recognition of right-sided MI begins with
diuretics, aldosterone antagonists, and -blockers. obtaining an electrocardiogram (ECG) and observing
Digoxin continues to be helpful in some of these pa- ST-segment elevation in leads II, III, and aVF, with or
tients. When patients present with end-stage heart fail- without accompanying abnormal Q waves. All patients
ure and are hypotensive, management is quite differ- with acute inferior wall MI should have an initial ECG
ent. Parenteral inotropic agents may be initiated. performed with the chest leads placed on the right
However, inotropic agents, such as dopamine and do- chest in mirror image fashion to those normally placed
butamine, may exacerbate myocardial ischemia by aug- on the left. ST-segment elevation in leads V3r and V4r is
menting inotropy and increasing heart rate (all major indicative of right ventricular MI.6 If right coronary
determinants of myocardial oxygen consumption). artery occlusion is proximal, it can produce associated
Amrinone and milrinone are often reserved for use findings such as PR-segment displacement, an indica-
when other agents have proven ineffective or when pa- tion of right atrial infarction, with or without sympto-
tients have significant evidence of -adrenergic block- matic bradycardia, atrioventricular (AV) nodal block,
ade, but these phosphodiesterase inhibitors may in- or atrial fibrillation.4 Echocardiographic evaluation
duce hypotension or arrhythmias. Vasodilators should usually reveals inferior wall motion abnormalities
be used with extreme caution in the acute decompen- along with a dilated and akinetic right ventricle.
sated setting. The same may be said for initiation of
-blockers in the setting of initial presentation with Treatment
severe volume overload and hypotension (so-called The initial medical treatment of isolated anterior or
wet-cold pathophysiology). Nitroprusside can de- inferior MI with borderline or stable hemodynamics
crease filling pressures and can increase stroke volume (beyond acute revascularization or in noncandidates)
by reducing afterload, but its use should be monitored might include anticoagulation, antiplatelet agents, di-
closely because it can exacerbate hypotension. Intra- uresis, afterload reduction, and preload reduction
aortic balloon pumping reduces systolic afterload and using intravenous nitrates, morphine, -blockers, and
augments diastolic perfusion pressure, thus increasing angiotensin-converting enzyme inhibitors.7 In contrast,
cardiac output and improving coronary blood flow. It the initial treatment of inferior MI with hypotension
also is a useful bridging intervention that allows thera- mandates volume resuscitation. In this particular in-
peutic measures, such as coronary revascularization or stance, preload reducers (eg, nitrates, vasodilators)
valvular surgery, to be undertaken.1,3 should be avoided. Intravenous inotropes are recom-
mended if volume infusion is unsuccessful in improving
RIGHT VENTRICULAR MYOCARDIAL INFARCTION cardiac output.4,8 Opening of the occluded coronary
Myocardial infarction (MI) is a major cause of car- artery is crucial. Early reperfusion with thrombolytics/
diogenic shock. Related complications, such as acute angioplasty/stenting/coronary artery bypass grafting
mitral regurgitation, rupture of interventricular sep- leads to prompt hemodynamic improvement and sub-
tum, and rupture of ventricular free wall, can produce sequent recovery of right ventricle free wall contractility.
severe hypotension. The present discussion mainly per- Because it is also important to maintain AV synchrony,
tains to right-sided MI because of this conditions asso- AV pacing for symptomatic bradycardia or advanced AV
ciation with both shock and JVD. The principle cause block may be indicated.

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 Chauhan & Schocken : Shock with JVD : pp. 17 24, 29

SHOCK

Jugular venous Differential diagnosis

Check breath sounds Present Absent
distension Septic shock
Present Absent Hypovolemia/hemorrhage
Neurogenic shock
Anaphylactic shock
Pneumothorax Drugs
Adrenal insufficiency
Check for crackles Present Consider AMI or CHF High-output failure
Hepatic failure
Absent

Check for heart sounds

Distant Tamponade
Normal

Low voltage
Tamponade

Further work-up S1Q3T3 pattern or

Check ECG Pulmonary embolism
with CXR and ECG sinus tachycardia
+ ST-segment
elevation
AMI CHF Normal

Pulmonary congestion
Cardiac malposition Echocardiogram
Cardiac postoperatively CXR Normal see Figure 2
herniation

Enlarged cardiac Pericardial

silhouette Pneumothorax calcification
with mediastinal
Tamponade shifting Constrictive pericarditis

Tension pneumothorax

Figure 1. Algorithm for the diagnosis of shock. AMI = acute myocardial infarction; CHF = congestive heart failure; CXR = chest
radiograph; ECG = electrocardiogram.

CARDIAC TAMPONADE orthopnea. On physical examination, pulsus paradox-

Tamponade is best thought of as a spectrum of us, JVD with rapid x descent, and distant heart sounds
pathophysiologic states rather than an all-or-nothing can be appreciated.9,10
phenomenon. Tamponade can present with as little as
50 mL of fluid in the pericardial space or as much as Pathophysiology
1 L or more of fluid, depending on the amount of time Physiologically, pericardial volume rises, causing a
over which the fluid collects. Tamponade can be idio- reduction in cardiac chamber volumes and a fall in dia-
pathic or can be caused by various different underlying stolic compliance in all chambers. These events translate
causes such as malignancy, trauma, thoracic surgery, to restriction of cardiac inflow and outflow. Continued
radiation, drugs (eg, cyclosporine), uremia, connective increases in pericardial pressure augment diastolic filling
tissue disease, infection, or complications of percuta- pressures to the point of decompensation. The hallmark
neous coronary intervention. Early symptoms may re- of pure cardiac tamponade is progressive reduction of
semble those of heart failure, including dyspnea and diastolic compliance with elevation and equalization of

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 Chauhan & Schocken : Shock with JVD : pp. 17 24, 29

Congestive heart failure Constrictive pericarditis

Left ventricle Pericardial

dilation/dysfunction thickening

Segmental wall
Myocardial infarction ECHOCARDIOGRAM Pericardial effusion Tamponade
motion abnormality

Intracardiac Dilated right

echodensity Postoperative ventricle
pericardial
Tumor or thrombus thrombus Pulmonary embolism

Pericardial thrombus

Figure 2. Algorithm depicting the utility of echocardiography in diagnosing the underlying cause in patients who present with
shock and jugular venous distention.

the mean diastolic pressures in all 4 chambers. At this PERICARDIAL THROMBUS

point, patients nearly always demonstrate pulsus para- Pericardial clot should always be considered in pa-
doxus on physical examination.912 tients who are hypotensive after cardiac surgery, blunt
trauma, or pericardiocentesis or who have a history of
Diagnostic Modalities bleeding disorder.14 16 Pericardial thrombus presents
The ECG in cardiac tamponade can reveal low voltage similarly to cardiac tamponade but may be indolent
electrical alternans and changes characteristic of peri- and can present up to 10 days postsurgery. Patients are
carditis. Without intervention, pulseless electrical activity usually tachycardic and hypotensive, with muffled
may ensue. The echocardiogram may reveal decreased heart sounds and significant JVD. Pulsus paradoxus
stroke volume with collapse of the right ventricular and may or may not be present. Although symptoms are
right atrial free walls in late diastole. Collapse of cham- vague, it is important to note the history and have
bers usually indicates decreasing cardiac output and im- a high clinical suspicion in postoperative or post-
pending tamponade.12,13 In the presence of tamponade, traumatic patients.15
cardiac Doppler ultrasonography reveals wide swings in Restriction of the heart by a localized mass in the
flow across the tricuspid and mitral valves throughout the pericardial space may cause atypical findings of com-
respiratory cycle. These flow variations are the central cir- pression of selected chambers by localized augmenta-
culatory equivalent of pulsus paradoxus. tion of intracardiac pressure, as in tamponade. Pericard-
ial thrombus may act as an elastic form of constrictive
Treatment pericarditis. A sharp early dip in right ventricular dia-
Pericardial drainage is the treatment of choice stolic pressure is followed by a rapid early increase in
when available, but medical supportive care, especially diastolic pressure abruptly ending in a plateau phase
volume expansion, may be applied when pericardio- (square-root sign).14 Compression of any or all cham-
centesis is not immediately available. Temporary use of bers has been noted. Tamponade after cardiac surgery is
inotropic agents is of minimal benefit because the frequently due to pericardial effusion or pericardial
problem is primarily one of diastolic function, not clots, often located posteriorly. Transthoracic echocar-
systolic function. ECG - and/or echocardiographic- diography (TTE) remains the initial diagnostic tool, but
guided pericardiocentesis can be approached via a sub- clots can very often be difficult to detect with TTE due
xiphoid or apical route. The underlying cause should to surgical wound dressings and mechanical ventila-
be treated to prevent recurrence of pericardial effu- tion.14,15 Therefore, transesophageal echocardiography
sion. Subxiphoid pericardial window is the procedure (TEE) may provide a better approach.17
of choice for malignant pericardial effusion or recur-
rent tamponade physiology. Prognosis depends on the Treatment
underlying etiology.13 Treatment options in patients who have pericardial

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 Chauhan & Schocken : Shock with JVD : pp. 17 24, 29

thrombosis and who have any evidence of hemodynam- respond well to -blockers and diuretics for relief of
ic deterioration are confined to surgical exploration. symptoms of systemic congestion. Surgery is the most
Removal of the compressing clot results in rapid hemo- effective treatment choice with either partial or com-
dynamic and symptomatic improvement.1418 plete pericardial stripping.

CONSTRICTIVE PERICARDITIS TENSION PNEUMOTHORAX

Constrictive pericarditis is an uncommon disorder Tension pneumothorax is a life-threatening condi-
characterized by impaired diastolic filling, disassociated tion that develops due to injury resulting in air leak into
ventricular function, and systemic venous congestion. but not out of the pleural space, usually from some type
Most cases occur after cardiovascular surgery, radiation of one-way valve mechanism. During inspiration, air
therapy, or tuberculosis infection. Usually patients pre- escapes into pleural space, but during expiration, the
sent with orthopnea, venous congestion, cachexia, and communication between lung and pleural space may
dyspnea, but advanced cases can present with hypoten- become occluded. Tension pneumothorax can develop
sion if cardiac output has deteriorated significantly due following barotrauma that occurs during mechanical
to ventricular underfilling. Physical examination dem- ventilation or during resuscitation, trauma, invasive pro-
onstrates JVD along with other signs of central and cedures, or lung resection or can be caused by sponta-
peripheral congestion, including ascites and edema. neous pneumothorax, tumors, and infection. In tension
Jugular venous pulsation is characterized by rapid x pneumothorax, the pleural space usually contains 1.5 L
and y descent along with Kussmauls sign (paradoxical to 2 L of air. Tension pneumothorax is heralded by a
increase of JVD with inspiration). Pericardial knock on sudden deterioration in cardiopulmonary status caused
cardiac auscultation is a pathognomonic sign of con- by markedly increased intrapleural pressure that leads to
strictive pericarditis.19 displacement of mediastinum, depressed diaphragm,
The pathophysiologic hallmark of constrictive peri- and compression of the heart and lungs.21,22
carditis is loss of pericardial compliance. The pericardi- Patients may initially complain only of chest pain,
um is thickened, encasing the heart. This process leads to and as their condition worsens, dyspnea and cyanosis
disassociation of intrathoracic and intracardiac pressures may become apparent. On physical examination, pa-
with respiration. Elevated end-diastolic right ventricular tients have JVD, hypotension, and hyperresonant per-
pressures restrict filling. Right ventricular pressure mea- cussion of lungs over the affected hemithorax. Most
surements disclose dip and plateau (square-root sign), notably, the trachea and heart are often shifted to the
indicating rapid early diastolic filling followed by lack of unaffected side.
additional filling. There is also discordance between right
ventricular and peak left ventricular systolic pressures Diagnostic Modalities
during inspiration.20 Chest radiography has a high diagnostic yield and is
the diagnostic tool of choice in most cases of tension
Diagnostic Imaging pneumothorax. Air in pleural cavity, diaphragm depres-
Echocardiogram is the diagnostic modality of choice sion, and contralateral deviation of mediastinal struc-
for constrictive pericarditis. Pericardial thickening tures are evidence of a tension pneumothorax. Com-
greater than 5 mm is usually indicative of constrictive puted tomography (CT) scanning is more sensitive and
pericarditis. Rapid early ventricular filling is represent- can be utilized (in noncritical patients) for diagnostic
ed on echocardiogram as a tall E wave on the mitral in- purposes when chest radiography is nonrevelatory, as is
flow Doppler signal. In addition, inflow velocities fall as the case in limited ventral tension pneumothorax.23
much as 25% to 40%, and conversely, tricuspid velocity Several ECG findings have been described in tension
increases in inspiration. Abrupt intraventricular septal pneumothorax, such as rightward axis deviation, dim-
bounce in early diastole also indicates rapid early fill- inution of precordial R wave, decreased QRS amplitude,
ing. The chest radiograph also has additional diagnostic and precordial T-wave inversion. These relatively non-
value if pericardial calcification is present. specific ECG changes have been attributed to either car-
diac axis changes or direct pressure on coronary arteries
Treatment from tension pneumothorax.24
Unrecognized cases of constrictive pericarditis can
advance until patients have signs of hypoperfusion due Treatment
to low cardiac output. Intravenous fluids can temporar- If there is suspicion of tension pneumothorax,
ily stabilize these patients. In contrast, stable patients management, including decompression, should be

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 Chauhan & Schocken : Shock with JVD : pp. 17 24, 29

approached urgently. Hemodynamically significant ten- Treatment

sion pneumothorax is treated with needle thoracostomy, Shock, which is not always present in this syndrome,
which is performed by inserting a catheter needle in the confers a worse prognosis.27 Therefore, patients with
second intercostal space in the midclavicular line. Needle suspected massive pulmonary embolism often require
thoracostomy always requires follow-up chest tube place- aggressive resuscitation and stabilization. Administra-
ment. If the condition does not resolve, open thoracosto- tion of supplemental oxygen and volume expansion
my must be performed to determine whether the lung with crystalloid are the initial management for hypox-
has a large air leak (eg, ruptured bronchus) requiring emia and hypotension, respectively. Fluid resuscitation
direct repair.22,25 should be monitored closely, since increased volume
can worsen an already volume-overloaded right ventri-
MASSIVE PULMONARY EMBOLISM cle. Heparin should be instituted in all pulmonary em-
Massive pulmonary embolism results when em- bolism patients unless contraindicated, and it should
bolism size and underlying cardiopulmonary status be titrated to achieve rapid therapeutic anticoagulation
interact to produce hemodynamic instability. Circu- to prevent recurrence.28 Thrombolytic therapy should
latory failure occurs in about 10% of patients with pul- be considered for patients with shock caused by mas-
monary thromboembolism. In acute pulmonary em- sive pulmonary embolism. Although thrombolytics
bolism, occlusion of 2 major pulmonary arteries is seem appealing, only 1 study has demonstrated a mor-
usually (but not always) required to create hemody- tality benefit.27 Thrombolytics are not indicated in
namic instability. However, elaboration of vasoactive patients without right ventricular overload. For hemo-
hormones by even small thromboemboli may produce dynamically unstable patients with a contraindication
vasomotor instability. Pulmonary embolism often to thrombolytic therapy who are refractory to medical
occurs in the setting of malignancy or recent history of treatment for over 1 hour or have ongoing cardiac
surgery, although 50% of pulmonary embolism occurs arrest, surgical embolectomy should be considered.26,27
in absence of such classic predisposing factors as im-
mobilization and pregnancy.26 RIGHT ATRIAL THROMBUS
Massive pulmonary emboli lead to rapid onset of Right atrial thrombi are uncommon but are often
circulatory failure and signs of acute cor pulmonale. clinically significant. Right atrial thrombi can be idiopath-
This critical state is often preceded by symptoms such ic or can be caused by many different processes, such as
as syncope, chest pain, dyspnea, and manifestations of atrial fibrillation, hypercoagulable state (eg, malignancy,
acute right heart failure (JVD and accentuated pul- antiphospholipid antibody, protein C deficiency), car-
monary S2). ECG may demonstrate various abnormali- diomyopathy, post-MI, central lines (including vascular
ties including right axis shift, tachycardia, S1Q 3T3 pat- access devices), Behets disease, pacemaker wire, and
tern, right bundle branch block, or diffuse T-wave shunts.2933 The symptoms and physical findings associat-
inversion.27 ed with this syndrome depend on the size and location of
the thrombus. Patients with right atrial thrombi may pre-
Diagnostic Imaging sent with dyspnea, chest pain, or syncope. Pulmonary
Suspected pulmonary embolism may be approached embolus is present in 98% of symptomatic cases, whereas
with a variety of imaging studies such as echocardiogra- hypotension and JVD are present in less than half of
phy, ventilation/perfusion scan, spiral CT scan, or pul- these symptomatic patients.34 Right atrial thrombi are
monary angiography. However, when a patient presents more likely to cause JVD rather than hemodynamic col-
with cardiovascular collapse due to massive pulmonary lapse. Regardless of their size, right atrial thrombi are
embolus, options are limited. The typical echocar- associated with significant tricuspid regurgitation, leading
diographic picture of a hemodynamically significant to at least a minor elevation of jugular venous pressure.
pulmonary embolus includes a dilated, hypokinetic Thrombus obstructing right ventricular inflow at the tri-
right ventricle with an increased right ventricle-to-left cuspid valve has been reported.31 33 Both pulmonary
ventricle-diameter ratio due to interventricular septal embolism and right heart outflow tract obstruction are
bulging into the left ventricle. Other findings include life-threatening complications of right atrial thrombus.
dilated pulmonary arteries, tricuspid regurgitation, and Primary thrombi intrinsic to the heart are more likely to
dilated inferior vena cava, all signs of acute rise in right be nonmobile and less likely to be complicated by pul-
ventricular pressure and volume. Hemodynamically monary embolism, whereas thrombi arising from sys-
important pulmonary embolus is unlikely in a patient temic veins are more likely to be mobile and carry higher
with a normal echocardiogram.26,27 risk of pulmonary embolism.35

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Diagnostic Imaging present with right heart failure accompanied by dyspnea,

Many diagnostic modalities for detecting right atrial JVD, hepatomegaly, S3, diastolic rumbles, and peripheral
thrombus have been studied. TTE remains the initial edema. Thirty percent of these patients may have had
diagnostic choice because of its simplicity, versatility, recent embolic events.41,42 Imaging with TEE or magnetic
and noninvasive approach.33 However, TTE is likely to resonance has proven effective in noninvasive detection
miss thrombi in the right atrial appendage, and this of intracardiac masses.43 Under emergent conditions,
shortcoming accounts for TTEs low sensitivity. TEE is TTE can provide anatomic and hemodynamic informa-
better than TTE at diagnosing right atrial thrombi.35 tion quickly, establishing the diagnosis and guiding treat-
One study indicated higher sensitivity of ultrafast CT ment. Myxomas usually appear as intracavitary peduncu-
scanning for visualization of right atrial thrombi com- lated (with stalk) or round masses on echocardiography
pared with TTE.36 A CT scan should be performed if (often arising in the area of the fossa ovalis), while meta-
there is a high clinical suspicion for thrombotic pathol- static malignancies are frequently associated with pericar-
ogy despite negative findings on echocardiogram.36,37 dial effusion.39,40 Metastatic intracavitary lesions are more
Digital subtraction angiography may also prove useful. likely to be on the right side of heart and may cause right
ventricular outflow tract obstruction.
Treatment
Because of the infrequency of patients presenting Treatment
with this condition, management of right atrial throm- Surgery is indicated for cure of benign tumors be-
bi has been individualized. Therapeutic measures cause they do not commonly recur after resection. Ma-
should be taken to prevent pulmonary embolism. If a lignant tumors (or multicentric benign tumors), on
large thrombus is the cause of shock, emergent surgery the other hand, have a poor prognosis since surgical
might be considered.32,34,38 Rose et al34 studied antico- approaches demand resection of significant portions
agulation, surgery, and thrombolysis as primary ap- of cardiac tissue. Palliative management should be
proaches to treatment, and they concluded that throm- directed at preventing embolic or arrhythmic phenom-
bolytics are superior to surgical intervention. The ena associated with cardiac malignancy.41
combination of platelet glycoprotein inhibitors and
heparin as a possible treatment option is currently CARDIAC HERNIATION
under investigation. Cardiac herniation is a rare cause of shock and is
usually a complication after pneumonectomy. Cardiac
CARDIAC TUMORS herniation has only been reported when the pericardi-
In addition to embolized thrombus, cardiac tumors um remains open after surgery. The heart protrudes
should be considered in the differential diagnosis of through the pericardial opening and occupies removed
shock with JVD. Metastatic malignancies are more lung space, which causes obstruction of outflow vessels,
common than primary cardiac tumors. Lung cancer thereby strangulating the myocardium. Most cases
and melanoma are the most common causes of meta- occur within 72 hours of the pneumonectomy. Signs and
static cardiac tumors, but renal cell tumors, breast tu- symptoms include acute hypotension, JVD, chest pain,
mors, and lymphomas are also well-documented sec- cyanosis, and sometimes superior vena cava syndrome.
ondary malignancies of the heart. Primary myxoma is Right-sided cardiac herniation can easily be con-
the most common primary benign tumor of the heart, firmed by simple chest radiography demonstrating a
whereas sarcomas (angiosarcoma, rhabdomyosarcoma, characteristically abnormal cardiac silhouette. However,
fibrosarcoma, leiomyosarcoma) are the most common left-sided cardiac herniation may be difficult to diagnose
primary invasive malignancies of the heart.39,40 Ex- without CT scan. Usually, these patients are unstable and
trinsic compression by tumors, such as mediastinal lym- may require surgical exploration. Treatment is surgical
phomas and bronchogenic carcinoma, have been re- repair of the pericardium. Even with intervention, car-
ported to present as right heart failure, chest pain, and diac herniation is associated with high mortality.44
hypotension with symptoms suggestive of tamponade
or pulmonary embolism. CONCLUSION
Cardiovascular collapse requires rapid assessment and
Diagnostic Imaging treatment. Delineating the underlying cause of shock
Cardiac tumors can result in cardiogenic shock by with JVD is essential for patient survival and maintaining
obstructing right atrial or ventricular outflow, thus lead- hemodynamic stability. A thorough history and detailed
ing to reduced cardiac output. These patients typically physical examination should be undertaken during the

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initial steps of the evaluation. In the absence of firmly after open heart surgery: its specific localization and
established accompanying pulmonary congestion, these haemodynamics. Eur Heart J 1993;14:2304.
15. Russo AM, OConnor WH, Waxman HL. Atypical pre-
patients are generally acceptable candidates for fluid
sentations and echocardiographic findings in patients
resuscitation while other data are being emergently gath-
with cardiac tamponade occurring early and late after
ered. The role of echocardiography is underutilized in cardiac surgery. Chest 1993;104:718.
critically ill patients. Emergent echocardiography should 16. DCruz IA, Kensey K, Campbell C, et al. Two-dimensional
be considered as a first-line diagnostic modality in pa- echocardiography in cardiac tamponade occurring after
tients presenting in shock with JVD. HP cardiac surgery. J Am Coll Cardiol 1985;5:12502.
17. Pierli C, Iadanza A, Del Pasqua A, Fineschi M. Acute
superior vena cava and right atrial tamponade in an
Test your knowledge and infant after open heart surgery [letter]. Int J Cardiol
comprehension of this article with 2002;83:1957.
Review Questions on page 36. 18. Calabrese P, Iliceto S, Rizzon P. Pericardiocentesis-
induced intrapericardial thrombus: visualization of
thrombus formation and spontaneous internal lysis by
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